Abstract
The dominant model for eukaryotic cell cycle control proposes that cell cycle progression is driven by a succession of CDK complexes with different substrate specificities. However, in fission yeast it has been shown that a single CDK complex generated by the fusion of the Cdc13 cyclin with the CDK protein Cdc2 can drive the mitotic cell cycle. Meiosis is a modified cell cycle programme in which a single S-phase is followed by two consecutive rounds of chromosome segregation. Here we systematically analyse the requirements of the different fission yeast cyclins for meiotic cell cycle progression. We also show that a single Cdc13–Cdc2 complex, in the absence of the other cyclins, can drive the meiotic cell cycle. We propose that qualitatively different CDK complexes are not absolutely required for cell cycle progression either during mitosis or meiosis, and that a single CDK complex can drive both cell cycle programmes.
Highlights
The dominant model for eukaryotic cell cycle control proposes that cell cycle progression is driven by a succession of cyclin-dependent protein kinase (CDK) complexes with different substrate specificities
The dominant model for eukaryotic cell cycle control is that there is a succession of different CDK complexes with different substrate specificities that appear at different stages of the mitotic cell cycle
These qualitatively different kinase complexes drive cells through G1, S-phase, G2 and mitosis and ensure there is a single S-phase each cell cycle[1,2,3]. This model has been challenged by work in fission yeast, where it has been shown that the four mitotic cell cycle CDK–cyclin complexes can be substituted by a single CDK–cyclin chimeric protein generated by the fusion of the Cdc[13] cyclin with the CDK protein Cdc[2]
Summary
Requirement of Cdc[13] cyclin during the meiotic cell cycle. In fission yeast, premeiotic S-phase, reductional meiosis I nuclear division and meiosis II require both mitotic- and meiotic-specific CDK–cyclin complexes[17,18,19]. Dyad formation on meiotic induction has been reported to be the result of mutations that compromise CDK activity, such as different cdc[2] thermo-sensitive alleles[4,25,26,27], or the deletion of the APC/C antagonist mes[1], which results in premature degradation of Cdc[13] at the end of meiosis I, preventing the cells undergoing a second meiotic division[21,22,23] Given these observations, we analysed the dynamics of Cdc13-Cdc[2] protein levels on induction of synchronous azygotic meiosis and compared them with the endogenous Cdc[13] and Cdc[2] in a wild-type strain. This probably led to an increase in the level of CDK activity as indicated by the reduction of cell size at division of these strains during the mitotic cell cycle when compared with single
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